Genetics of Antibiotics-Induced Liver Injury
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Antibiotics are commonly prescribed medications used to treat bacterial infections. While antibiotics can be very effective at killing off harmful bacteria, they can sometimes cause unintended damage to the liver, known as drug-induced liver injury (DILI).
DILI from antibiotics appears to be relatively uncommon; however, it remains a concern, particularly for certain higher-risk antibiotics. The antibiotics most associated with liver injury are tetracyclines, amoxicillin-clavulanate, fluoroquinolones, and sulfonamides.
The mechanisms behind antibiotic-induced liver damage are not entirely clear but likely involve an abnormal immune reaction. Antibiotics disrupt the normal gut bacteria, and this may allow intestinal bacteria that would normally be suppressed to proliferate and trigger inflammation. Another theory is that antibiotic metabolites directly inflict oxidative stress and damage to liver cells. Genetic factors likely also play a role, as some patients appear more susceptible to DILI than others when taking the same antibiotic.
Our liver helps process and clear antibiotics from the body. Differences in liver genes can cause some people to break down medications slower. This allows antibiotics to build up to toxic levels that injure liver cells. Other gene changes may lead to an abnormal immune reaction that attacks the liver. Genetic factors also impact how our bodies handle oxidative stress from antibiotics.
The symptoms of antibiotic-associated DILI can include nausea, fatigue, jaundice (yellowing of skin and eyes), light-colored stools, dark urine, and right upper abdominal discomfort. Symptoms typically arise within 3 months of starting an antibiotic. Mild cases may resolve within a few weeks of stopping the medication, but severe injury can lead to liver failure, requiring transplant.
A 2021 study found the antibiotic amoxicillin-clavulanate to have the highest risk of liver injury, with 15 cases per 100,000 exposures. Meanwhile, sulfamethoxazole-trimethoprim, levofloxacin, and nitrofurantoin were also flagged as moderate-risk antibiotics. Tetracyclines as a class have been linked to DILI, but doxycycline may be safer than other tetracyclines.
If antibiotic-induced liver injury is caught early, the best treatment is prompt withdrawal of the offending medication. Patients are advised to seek immediate medical care if they develop jaundice or other symptoms while on antibiotics. To reduce the need for antibiotics, some natural alternatives include probiotics, garlic, cranberry, and goldenseal. However, antibiotics should not be stopped without medical oversight.
Careful monitoring of liver tests is recommended for those at higher risk of DILI, including the elderly, those who drink regularly, and patients on multiple medications. Preventative measures include choosing lower-risk antibiotic options when possible, using the shortest effective antibiotic course, and avoiding unnecessary antibiotics for viral illnesses. Being aware of early symptoms of liver injury may help avoid progression to more serious damage.
In summary, while rare, certain widely used antibiotics have been associated with liver injury. Seeking prompt medical attention for new symptoms while on antibiotics, being aware of higher-risk drugs, and exploring antibiotic alternatives when appropriate may help reduce the likelihood of this dangerous complication. With careful prescribing and monitoring, antibiotics can be used safely, even in higher-risk patients.
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Green tea extract
Contains catechins which may increase oxidative stress and liver cell damage when combined with hepatotoxic antibiotics.
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Greater celandine
Alkaloids like chelidonine may further impair liver function when the organ is under stress from antibiotics.
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Chaparral
Nordamnacanthal is a quinone that could synergistically increase antibiotic liver toxicity through mitochondrial dysfunction.
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Germander
Diterpenoids may amplify antibiotic liver injury by disrupting bile salt export and causing cholestasis.
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Mistletoe
Contains toxic lectins which could worsen immunological reactions or alter detox pathways of antibiotic metabolites.
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Skullcap
Flavonoids may inhibit pathways involved in hepatic metabolism and clearance of antibiotics from the liver.
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Valerian
Isovaltrate and other constituents thought to directly damage cell membranes, potentially worsening antibiotic hepatocellular toxicity.
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Kava kava
Kavalactones like desmethoxyyangonin may inhibit CYP450 liver enzymes important for antibiotic clearance.
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St. John's wort
Hyperforin alters PXR nuclear receptors and could decrease bile acid transport, contributing to antibiotic cholestasis.
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Ginseng
Ginsenosides may inhibit P-glycoprotein transporters important for antibiotic efflux from hepatocytes, allowing accumulation of toxic levels.
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Aloe vera
Anthraquinone glycosides possibly damage cell membranes and worsen antibiotic-mediated liver cell necrosis.
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Ashwagandha
Withanolides thought to cause oxidative stress which synergizes with redox-cycling antibiotic metabolites.
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Andrographis
Diterpene lactones may reduce bile acid secretion and flow, contributing to cholestatic injury.
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Noni juice
Anthraquinones could impair mitochondrial function and increase antibiotic hepatotoxicity.
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Peppermint oil
Menthol interferes with CYP450s and UGTs involved in antibiotic metabolism and clearance.
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Kratom
Mitragynine and 7-hydroxymitragynine are metabolized in liver and could enhance antibiotic toxicity.
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Ephedra
Ephedrine alkaloids may deplete glutathione and reduce the liver's defense against antibiotic oxidative damage.
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